Objective To explore the mechanism of the inhibitory effect of microRNA ( miR)-1247 onlipopolysaccharide (LPS)-induced acute pneumonia. Methods Thirty 8-week-old female BABL/ c mice were randomlydivided into three groups: acute pneumonia model group (6 h), acute pneumonia model group (12 h) and normal group,with 10 mice in each group. LPS solution (8 mg/ kg) was instilled into the mouse trachea of the model group, and thenormal group was instilled an equal volume of physiological saline. Autopsy was performed after anesthesia at 6 h and 12 hafter LPS modeling. The blood gas from the celiac artery was measured. The dry and wet weight of lung tissue was measured.qRT-PCR and ELISA were used to detect the expression levels of TNF-α, IL-1β and miR-1247 in the pulmonary tissues.The levels of CCR16, TLR4, IRAK6, TAK, IKK and NF-κB p52 proteins in the lung tissues of each group were detectedby western blot. Results Compared with the normal group, the PaO₂, oxygen index (PaO₂ / FiO₂ ) of the model groupmice was decreased, and the dry-wet weight ratio of the lung was significantly increased ( P < 0.05). However, thedifferences in PaCO₂ and mRNA expression levels of TNF-α and IL-1β between the two groups were not statisticallysignificant ( P > 0.05). The levels of miR-1247 and CCR16 protein expression in the lung tissues of the model group weresignificantly increased at 6 h and 12 h after modeling ( P < 0.05). Compared with the normal group, the expression ofTLR4 on the cell surface was significantly lower ( P < 0.05). Compared with the normal group, the expressions of IRAK6,TAK, IKK and transfected nuclear protein NF-κB in the tissues at 6 h and 12 h after modeling were decreased significantly( P < 0.05).Conclusions The results of this study show that miR-1247 inhibites the increase of various cytokines and proteins in the LPS-induced acute pneumonia model via chemokine ligand CCR16.